Lp(a) is a low-density lipoprotein which is structurally similar to plasminogen. Although it competes for plasminogen binding sites, it is not cleaved to plasmin by t-PA. In vitro studies suggest an association between elevated Lp(a) serum concentrations and altered fibrinolysis. In vivo data is lacking. Thyroid hormones stimulate synthesis, mobilization, and degradation of plasma lipids, including Lp (a). The natural course of current thyroid cancer management predisposes patients to definite and often extreme fluctuations in thyroid hormone levels, making this population potentially useful for observing maximal thyroid hormone- induced changes in Lp(a). This open-label, pilot trial involves a total of twenty-two thyroid cancer patients receiving levothyroxine suppression therapy who are scheduled for radioiodine scanning. The study will evaluate the effects of thyroid hormone-induced changes in plasma Lp(a) concentration on hemostasis. Patients will discontinue levothyroxine and triiodothyronine therapy 6 and 2 weeks prior to the thyroid scan, respectively. Hemostatic parameters will be assessed at baseline (while receiving suppression therapy), at the time of scan (clinically hypothyroid), and after weeks l and 6 of restarting full-dose thyroid hormone treatment.